ライフサイエンスコーパス: spastic

1 al: 6.02 +/- 0.49 mm, p = 0.038; compliance: spastic: 1.79 +/- 0.12 mm/N, contralateral: 2.21 +/- 0.1

2 the contralateral side (muscle displacement: spastic: 4.84 +/- 0.33 mm, contralateral: 6.02 +/- 0.49

3 24; 2.2% overall) were ultimately managed as spastic achalasia or DES.

4 achalasia, achalasia with pressurization, or spastic achalasia with differential responses to treatme

5 pathophysiology: DES with short latency and spastic achalasia.

6 phageal compression and pseudorelaxation, or spastic achalasia.

7 At the opposite extreme is type III (spastic) achalasia, which has no demonstrated neuronal l

8 Thus, the spastic allele of the murine glycine receptor beta subun

9 , the initial progressive upper motor neuron spastic and general proprioceptive ataxia in the pelvic

10 d/or non-febrile seizures, and a wide-based, spastic, and/or stiff-legged gait.

11 scopic analyses of spinal cord sections from spastic animals revealed increased GluR1 immunoreactivit

12 t analyses of lumbar spinal cord tissue from spastic animals showed a significant increase in GluR1 b

13 n patients show a combination of adult-onset spastic ataxia and a thin corpus callosum.

14 considered in the differential diagnosis of spastic ataxia and hypomyelination.

15 ests GBA2 mutations are a cause of recessive spastic ataxia and responsible for a form of glucosylcer

16 ole-exome sequencing findings in a recessive spastic ataxia family turned our attention to intronic v

17 ochondrial DNA maintenance is suspected when spastic ataxia is prominent.

18 eurodegenerative disease autosomal recessive spastic ataxia of Charlevoix Saguenay (ARSACS) is caused

19 Autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) is a chil

20 Autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) is caused

21 Autosomal Recessive Spastic Ataxia of Charlevoix-Saguenay (ARSACS) is caused

22 n sacsin responsible for autosomal recessive spastic ataxia of Charlevoix-Saguenay, a degenerative di

23 d in the neurodegenerative disorder known as spastic ataxia of Charlevoix-Saguenay, and thus, we term

24 eurodegenerative disease autosomal recessive spastic ataxia of Charlevoix-Saguenay, is a node in this

25 nt with the diagnosis of autosomal recessive spastic ataxia of Charlevoix-Saguenay.

26 disorders that are classified either as pure spastic ataxia or as complex spastic ataxia with additio

27 the differential diagnosis of patients with spastic ataxia phenotype.

28 A total of 321 index patients with spastic ataxia selected from the SPATAX network were ana

29 either as pure spastic ataxia or as complex spastic ataxia with additional neurological signs.

30 haracterized by adolescent-onset progressive spastic ataxia with frequent occurrence of tremor, invol

31 d MARS2 to be mutated in Autosomal Recessive Spastic Ataxia with Leukoencephalopathy (ARSAL) patients

32 ular investigation of an autosomal-recessive spastic ataxia with optic atrophy, present among the Old

33 has previously been implicated in a form of spastic ataxia with optic atrophy.

34 ting features on MRI are sometimes seen with spastic ataxia, but this is usually mild in adults and s

35 gressive external ophthalmoplegia/ptosis and spastic ataxia, or a progressive ataxic disorder.

36 linked to spinocerebellar ataxia type 28 and spastic ataxia-neuropathy syndrome in humans; however, t

37 as significantly enriched in 1139 cases with spastic ataxia-related phenotypes as compared to unrelat

38 report seven individuals with an early-onset spastic-ataxia phenotype.

39 in POLR3A are a frequent cause of hereditary spastic ataxias, accounting for about 3% of hitherto gen

40 gnosed in 22% of infants; half of these were spastic bilateral.

41 The glycine receptor-deficient mutant mouse spastic carries a full-length long interspersed nuclear

42 caldesmon, and heat shock protein 27 in the spastic cerebral arteries at 24 hours post-SAH.

43 r-OPN induced MKP-1 in the spastic cerebral arteries via binding to L-arginyl-glycy

44 to a reduction in the frequency of bilateral spastic cerebral palsy among infants of birthweight 1000

45 Forty-nine children aged 3 to 8 years with spastic cerebral palsy were randomized to 40 treatments

46 1426 (94%) had spastic cerebral palsy, which was unilateral (hemiplegic

47 omic or physiologic CP subtype, diplegic and spastic children were more often hyperopic and esotropic

48 The resistance due to spastic co-contraction might be reduced by botulinum tox

49 tween luminal pressurization attributable to spastic contractions and that resultant from a trapped b

50 I (absent peristalsis with distal esophageal spastic contractions) is a spastic variant with less fav

51 ssociated with both unilateral and bilateral spastic CP subphenotypes.

52 ted for evaluation and further management of spastic diplegia cerebral palsy.

53 ncy include elevated plasma arginine levels, spastic diplegia, intellectual disability, seizures and

54 e disorder associated with hyperargininemia, spastic diplegia, loss of ambulation, intellectual disab

55 otypes: without peristalsis, with premature (spastic) distal esophageal contractions, with panesophag

56 nt alternatives for patients with achalasia, spastic esophageal disorders and upper gastrointestinal

57 ia and 90% of patients with type 3 achalasia/spastic esophageal motility disorders, with a low rate o

58 presses neuronal excitability and results in spastic flies.

59 ond most common type of cerebral palsy after spastic forms.

60 lthough more than 50 genetic loci are known [spastic gait (SPG)1 to -57], over half of hereditary spa

61 n disorders with the hallmark of progressive spastic gait disturbance.

62 acterized by neurogenic bladder, progressive spastic gait, and peripheral neuropathy.

63 Our laboratory utilized mutant spastic Han-Wistar rats (sHW) that display developmental

64 ith multiorgan IgG4-RD developed progressive spastic hemiparesis and dementia.

65 gical disorders characterized principally by spastic lower extremity weakness due to a length-depende

66 (DeltaNLS-FUS), which developed progressive spastic motor deficits and neuronal loss in the motor co

67 to its treatment) remains unknown, although spastic motor dysfunction has been related to the hypere

68 ortical motor neurons degenerate and cause a spastic movement disorder.

69 of muscle displacement and compliance in the spastic muscles as compared to the contralateral side (m

70 dendritic stratification patterns of RGCs in Spastic mutant mice, in which the OFF signal transmissio

71 However, the adult Spastic mutants had altered RGC light-evoked synaptic in

72 Moreover, light deprivation of the Spastic mutants had no additional impact on the RGC dend

73 Spastic mutation also blocked the developmental redistri

74 chart review, and comprised all infants with spastic or dyskinetic CP not caused by developmental abn

75 They are characterized by progressive spastic paralysis of the legs as a result of selective,

76 Tetanus toxin (TeNT) elicits spastic paralysis through the cleavage of vesicle-associ

77 evere clinical dysfunction with an ascending spastic paralysis ultimately resulting in fatal respirat

78 eoathetoid movements, dysarthria, dysphagia, spastic paralysis, and behavioral dementia in descendant

79 ease in the central nervous system to elicit spastic paralysis, but the molecular basis for TeNT entr

80 G) and tetanus neurotoxin elicit flaccid and spastic paralysis, respectively.

81 n the central nervous system (CNS) to elicit spastic paralysis.

82 neurons and protected mice from TeNT-induced spastic paralysis.

83 e BoNTs cause flaccid paralysis, TeNT causes spastic paralysis.

84 eral sclerosis and infantile-onset ascending spastic paralysis.

85 isease HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and adult T cell leukemia/

86 pe 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and multiple sclerosis (MS

87 us 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and multiple sclerosis (MS

88 pe I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) are known to be caused by

89 pe I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) exhibit reduced Foxp3 expr

90 pe 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a progressive inflammat

91 ent of HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), a chronic inflammatory di

92 ent of HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), observed in up to 5% of i

93 L) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP).

94 L) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP).

95 termed HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP).

96 sorder HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP).

97 pe I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP).

98 L) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP).

99 We studied a case of Hereditary Spastic Paraparesis (HSP) in a single inbred Palestinian

100 nia and parkinsonism (n = 1), and hereditary spastic paraparesis (n = 1).

101 ia and HTLV-1-associated myelopathy/tropical spastic paraparesis after the initial infection.

102 eases: HTLV-1-associated myelopathy/tropical spastic paraparesis and adult T cell leukemia.

103 ed with a similar combination of progressive spastic paraparesis and polyneuropathy, variably associa

104 FR deficiency is a rare cause of complicated spastic paraparesis in adults, it should be considered i

105 identified novel clinical presentations with spastic paraparesis mimicking hereditary spastic paraple

106 a complicated form of adult-onset hereditary spastic paraparesis partially responsive to betaine ther

107 rmines HTLV-1-associated myelopathy/tropical spastic paraparesis risk.

108 s with HTLV-1-associated myelopathy/tropical spastic paraparesis than in 29 asymptomatic carriers (80

109 isease HTLV-1-associated myelopathy/tropical spastic paraparesis was associated with significantly in

110 sive neurodegenerative subtype of lower limb spastic paraparesis with additional diffuse skin and hai

111 is mutated, patients frequently present with spastic paraparesis, a thin corpus callosum, and cogniti

112 kemia virus-1-associated myelopathy/tropical spastic paraparesis, A6 also recognizes a self peptide f

113 ropic virus I-associated myelopathy/tropical spastic paraparesis, rheumatoid arthritis, multiple scle

114 result in debilitating leukodystrophies and spastic paraparesis.

115 ia and HTLV-1-associated myelopathy/tropical spastic paraparesis.

116 ma and HTLV-1-associated myelopathy/tropical spastic paraparesis.

117 tive motor neuron disorders characterized by spastic paraparesis.

118 progressive gait ataxia with a superimposed spastic paraparesis.

119 in Reep1 null mice in addition to prominent spastic paraparesis.

120 and the neurodegenerative disorder tropical spastic paraparesis/HTLV-1-associated myelopathy (TSP/HA

121 adult T-cell leukemia/lymphoma and tropical spastic paraparesis/HTLV-1-associated myelopathy in abou

122 T-cell leukemia/lymphoma as well as tropical spastic paraparesis/HTLV-1-associated myelopathy.

123 , such as adult T-cell leukemia and tropical spastic paraparesis/myelopathy.

124 d with HTLV-1-associated myelopathy/tropical spastic paraparesis?

125 rative disease autosomal dominant-hereditary spastic paraplegia (AD-HSP).

126 lt in similar problems that cause hereditary spastic paraplegia (HSP) and Charcot-Marie-Tooth type 2

127 of upper and lower motor neurons, hereditary spastic paraplegia (HSP) and distal hereditary motor neu

128 autosomal recessive (AR) complex hereditary spastic paraplegia (HSP) and juvenile onset amyotrophic

129 Two syndromes - hereditary spastic paraplegia (HSP) and mycobacterial disease - thu

130 itary cerebellar ataxia (HCA) and hereditary spastic paraplegia (HSP) are scarce.

131 yndrome is an autosomal recessive hereditary spastic paraplegia (HSP) caused by frameshift mutations

132 Hereditary spastic paraplegia (HSP) comprises a group of clinically

133 Hereditary spastic paraplegia (HSP) describes a heterogeneous group

134 Complex hereditary spastic paraplegia (HSP) is a genetic disorder that caus

135 Hereditary spastic paraplegia (HSP) is a neurological syndrome char

136 Hereditary spastic paraplegia (HSP) type 2 is a proteolipid protein

137 its four subunits cause a form of hereditary spastic paraplegia (HSP) with intellectual disability.

138 stin, strumpellin, or REEP1 cause hereditary spastic paraplegia (HSP), a disease characterized by axo

139 in an autosomal dominant form of hereditary spastic paraplegia (HSP), a motor-neurological disorder

140 e an unbranched ER morphology and hereditary spastic paraplegia (HSP), a neurodegenerative disease ch

141 stin are the most common cause of hereditary spastic paraplegia (HSP), a neurodegenerative disease th

142 tified in patients suffering from hereditary spastic paraplegia (HSP), a neurodegenerative disorder a

143 Mutations of various genes cause hereditary spastic paraplegia (HSP), a neurological disease involvi

144 plex, have been reported to cause hereditary spastic paraplegia (HSP), although their impact at the c

145 hy (SMA), Multiple Sclerosis (MS) Hereditary Spastic Paraplegia (HSP), and Huntington's Disease (HD).

146 cot-Marie-Tooth disease (CMT) and Hereditary Spastic Paraplegia (HSP), but the mechanism of its invol

147 In hereditary spastic paraplegia (HSP), the axons of cortical motor ne

148 tReact effect in humans with pure hereditary spastic paraplegia (HSP).

149 use an axon degenerative disease, hereditary spastic paraplegia (HSP).

150 ing spastin and atlastin, lead to hereditary spastic paraplegia (HSP).

151 in produces similar phenotypes of hereditary spastic paraplegia (mitochondrial dysfunction and defect

152 HD2 genes cause specific types of hereditary spastic paraplegia (SPG28 and SPG54, respectively), and

153 been identified in both a form of hereditary spastic paraplegia (SPG35) and a progressive familial le

154 ns in kinesin family member 5A (KIF5A) cause spastic paraplegia 10.

155 otypic ER-shaping proteins, in families with spastic paraplegia 12 (SPG12).

156 and splice-site) associated with hereditary spastic paraplegia 4 (HSP-SPG4) (SPG4:OMIM#182601) has s

157 (mutations in which cause autosomal-dominant spastic paraplegia 4 [SPG4]) have been described, their

158 dentified a necessary and conserved role for spastic paraplegia 7 (SPG7) in Ca(2+)- and ROS-induced P

159 encoding a later step, result in hereditary spastic paraplegia accompanied by intellectual deficits.

160 sense mutations in AP5Z1 and presenting with spastic paraplegia accompanied by neuropathy, parkinsoni

161 eration: many candidate genes for hereditary spastic paraplegia also have central roles in lipid-drop

162 tified in genes usually associated with pure spastic paraplegia and also in the Parkinson's disease-a

163 Next, we screened a cohort of hereditary spastic paraplegia and cerebellar ataxia cases (n = 618)

164 in genetic neurological diseases (hereditary spastic paraplegia and cerebellar ataxia).

165 POLR3A to be a frequent cause of hereditary spastic paraplegia and cerebellar ataxia.

166 e fusion gene data could explain a report of spastic paraplegia and dementia cosegregating in a famil

167 hich affected subjects exhibited progressive spastic paraplegia and distal muscle wasting.

168 patients suffering from SPG4-type hereditary spastic paraplegia and explain why single amino acid exc

169 in neurological disorders such as hereditary spastic paraplegia and hereditary sensory neuropathy.

170 erosis, infantile-onset ascending hereditary spastic paraplegia and juvenile primary lateral sclerosi

171 ns with intellectual disability, progressive spastic paraplegia and short stature, born to a consangu

172 fficking is a common theme between heritable spastic paraplegia and some inherited epilepsies.

173 e: amyotrophic lateral sclerosis, hereditary spastic paraplegia and spinal muscular atrophy.

174 in NTE have been shown to cause a Hereditary Spastic Paraplegia called NTE-related Motor-Neuron Disor

175 l longer axons, and support a model in which spastic paraplegia can be caused by impairment of axonal

176 gait (SPG)1 to -57], over half of hereditary spastic paraplegia cases are caused by pathogenic mutati

177 yndrome is an autosomal recessive hereditary spastic paraplegia caused by mutation in the spartin (SP

178 Mutations in PNPLA6 also cause human spastic paraplegia characterized by motor neuron degener

179 Several causative genes for hereditary spastic paraplegia encode proteins with intramembrane ha

180 o most common autosomal recessive hereditary spastic paraplegia gene products, the SPG15 protein spas

181 Mutations in the Spastic Paraplegia Gene11 (SPG11), encoding spatacsin, c

182 ns in several loci known collectively as the spastic paraplegia genes (SPGs).

183 variants in a number of other known complex spastic paraplegia genes, including five in SPG7 (5/97),

184 and by far the most common cause of complex spastic paraplegia in the UK, with severe and progressiv

185 Hereditary spastic paraplegia is a highly heterogeneous group of ne

186 Clinical data showed that spastic paraplegia is accompanied by a number of other f

187 form of pure, autosomal dominant hereditary spastic paraplegia is caused by mutation in the ATL1 gen

188 ommon form of autosomal recessive hereditary spastic paraplegia is caused by mutations in the SPG11/K

189 assified as either 'pure' or 'complex' where spastic paraplegia is complicated with additional neurol

190 nant lower limb spasticity, or complex where spastic paraplegia is complicated with additional neurol

191 tion is the main regulator of the hereditary spastic paraplegia microtubule severing enzyme spastin.

192 functional defects of an atypical hereditary spastic paraplegia mutant, ATL1-F151S, that is impaired

193 h the microtubule cytoskeleton in hereditary spastic paraplegia pathogenesis.

194 rise from mutations identified in hereditary spastic paraplegia patients.

195 rst demonstration of a role for a hereditary spastic paraplegia protein or ichthyin family member in

196 ional progression rate of 0.56 points on the Spastic Paraplegia Rating Scale per year was slightly lo

197 Clinical severity was assessed by the Spastic Paraplegia Rating Scale.

198 ated a series of 97 index cases with complex spastic paraplegia referred to a tertiary referral neuro

199 nd implies disease mechanisms for hereditary spastic paraplegia that involve dependence of the microt

200 Motor signs developed ascending from spastic paraplegia to tetraplegia and pseudobulbar palsy

201 Spastic paraplegia type 5 (SPG5) is a rare subtype of he

202 nder investigation; recent studies show that spastic paraplegia type 5, a progressive neuropathy, is

203 Spastic paraplegia types 4 (prevalence, 0.91 per 100,000

204 patients with adult onset leukodystrophy or spastic paraplegia with early onset of urinary symptoms

205 utations, and predominant complex hereditary spastic paraplegia with marked cognitive impairment, wit

206 es related to autosomal recessive hereditary spastic paraplegia with thin corpus callosum and axonal

207 uent cause of autosomal recessive hereditary spastic paraplegia with thin corpus callosum and periphe

208 cal findings were neurogenic bladder (100%), spastic paraplegia with vibration loss (90%), and axonal

209 ity Gene2) and Bhlhb5 (mutated in Hereditary Spastic Paraplegia), providing a molecular handle to inv

210 sociated with various subtypes of hereditary spastic paraplegia, a highly heterogeneous group of neur

211 ype 5 (SPG5) is a rare subtype of hereditary spastic paraplegia, a highly heterogeneous group of neur

212 bone and frontotemporal dementia, hereditary spastic paraplegia, and 1-2% of familial amyotrophic lat

213 ith spastic paraparesis mimicking hereditary spastic paraplegia, and a multiple sclerosis-like illnes

214 um hypoplasia, retardation, adducted thumbs, spastic paraplegia, and hydrocephalus).

215 n is mutated in the human disease hereditary spastic paraplegia, and its link to WASH suggests that m

216 in the neurodegenerative disease hereditary spastic paraplegia, and of ichthyin, mutated in autosoma

217 autonomic neuropathy, complicated hereditary spastic paraplegia, and select hereditary metabolic neur

218 ions were found in patients with ichthyosis, spastic paraplegia, and severe neurodevelopmental defect

219 utosomal dominant pure or complex hereditary spastic paraplegia, as well as in two sporadic patients.

220 assified as a complicated form of hereditary spastic paraplegia, associated with mutation in the etha

221 ven to these patients included dementia with spastic paraplegia, corticobasal degeneration syndrome,

222 ave been linked to diseases such as familial spastic paraplegia, developmental delay with premature d

223 neuromuscular diseases including hereditary spastic paraplegia, hereditary sensory neuropathy type 1

224 set seizures, severe developmental delay and spastic paraplegia, in whom whole-genome sequencing reve

225 INS220/ARMS in three unrelated patients with spastic paraplegia, intellectual disability, nystagmus,

226 ghter, muscular hypotonia that progressed to spastic paraplegia, microcephaly, foot deformity, decrea

227 egenerative disorder mainly characterized by spastic paraplegia, optic atrophy and neuropathy (SPOAN)

228 have the unusual combination of early-onset spastic paraplegia, optic atrophy, and neuropathy.

229 in the clinico-genetic work-up of hereditary spastic paraplegia, particularly in dominant cases, as t

230 , parkinsonism, muscle weakness, neuropathy, spastic paraplegia, personality/behavioral problems, and

231 y classified as a complex form of hereditary spastic paraplegia, present in families from Kuwait, Ita

232 in the neurodegenerative disease hereditary spastic paraplegia, severs microtubules.

233 that are mutated in patients with hereditary spastic paraplegia, SPG11 and SPG15.

234 lity syndrome, and three forms of hereditary spastic paraplegia, SPG11, SPG15 and SPG49 caused by SPG

235 had normal development with childhood-onset spastic paraplegia, spinal lesion, and optic atrophy.

236 mutations cause a common form of hereditary spastic paraplegia, we suggest ER-shaping defects as a n

237 late-onset, slowly progressive, complicated spastic paraplegia, with normal or near-normal psychomot

238 ly progressive type of cerebellar ataxia and spastic paraplegia, without intellectual disability.

239 developmental defects and a familial form of spastic paraplegia.

240 has been associated with a familial form of spastic paraplegia.

241 stin are the most common cause of hereditary spastic paraplegia.

242 e human gene mutated in a form of hereditary spastic paraplegia.

243 stin is mutated in the axonopathy hereditary spastic paraplegia.

244 amyotrophic lateral sclerosis and hereditary spastic paraplegia.

245 PG3A, a common autosomal dominant hereditary spastic paraplegia.

246 e usual clinical presentation of progressive spastic paraplegia.

247 irst causal treatment strategy in hereditary spastic paraplegia.

248 tin, is the chief gene mutated in hereditary spastic paraplegia.

249 over time show progressive motor symptoms, a spastic paraplegia.

250 od model system for understanding hereditary spastic paraplegia.

251 dered the most frequent metabolic hereditary spastic paraplegia.

252 e, highlighting the genetic heterogeneity of spastic paraplegia.

253 s, consistent with a diagnosis of hereditary spastic paraplegia.

254 to motor neuron diseases, such as hereditary spastic paraplegia.

255 uting factor to early autonomic symptoms and spastic paraplegia.

256 r ataxias and autosomal recessive hereditary spastic paraplegias (ARHSPs) are clinically and genetica

257 The hereditary spastic paraplegias (HSPs) (SPG1-29) comprise a group of

258 The hereditary spastic paraplegias (HSPs) are a genetically and clinica

259 Hereditary spastic paraplegias (HSPs) are a group of diseases cause

260 Hereditary spastic paraplegias (HSPs) are a group of genetically he

261 Hereditary spastic paraplegias (HSPs) are a large, genetically dive

262 The hereditary spastic paraplegias (HSPs) are a rare and heterogeneous

263 The hereditary spastic paraplegias (HSPs) are characterized by spastici

264 Hereditary spastic paraplegias (HSPs) are clinically and geneticall

265 The hereditary spastic paraplegias (HSPs) are genetic conditions charac

266 Hereditary spastic paraplegias (HSPs) are genetically driven disord

267 The hereditary spastic paraplegias (HSPs) are heterogeneous neurodegene

268 Hereditary spastic paraplegias (HSPs) are neurodegenerative motor n

269 The family of genes implicated in hereditary spastic paraplegias (HSPs) is quickly expanding, mostly

270 ein 1 (REEP1) are associated with hereditary spastic paraplegias (HSPs).

271 drome, one of several complicated hereditary spastic paraplegias (HSPs).

272 Hereditary spastic paraplegias (HSPs, SPG1-46) are inherited neurol

273 Hereditary spastic paraplegias (HSPs; SPG1-45) are inherited neurol

274 Hereditary spastic paraplegias (HSPs; SPG1-48) are inherited neurol

275 Hereditary spastic paraplegias (HSPs; SPG1-76 plus others) are leng

276 The hereditary spastic paraplegias (SPG1-33) comprise a cluster of inhe

277 h rare movement disorders such as hereditary spastic paraplegias and cerebellar ataxias remain geneti

278 Hereditary spastic paraplegias are a clinically and genetically het

279 The hereditary spastic paraplegias are a heterogeneous group of degener

280 Hereditary spastic paraplegias are a large, diverse group of neurol

281 Hereditary spastic paraplegias are heterogeneous neurological disor

282 Hereditary spastic paraplegias are inherited neurological disorders

283 Complex recessive spastic paraplegias have in the past been frequently ass

284 been identified in patients with hereditary spastic paraplegias, a diverse group of neurological dis

285 ost common locus for mutations in hereditary spastic paraplegias, and katanin are related microtubule

286 gical disorders, particularly the hereditary spastic paraplegias, emphasizing the importance of prope

287 h define a diverse set of complex hereditary spastic paraplegias.

288 different neurological diseases, hereditary spastic paresis type 5 (SPG5) and cerebrotendinous xanth

289 Future research into the treatment of spastic paresis with botulinum toxin should use active m

290 SPG5 is characterized by spastic paresis, and similar symptoms may occur in CTX.

291 splay developmental abnormalities, including spastic paresis, fore limb tremors, hind limb rigidity,

292 2 to 4 months with progressive microcephaly, spastic quadriparesis, and global developmental delay.

293 typically, affected family members exhibited spastic quadriparesis, ataxia, and dystonia with onset i

294 stonia (DYT4), isolated hypomyelination with spastic quadriplegia, and an infantile onset encephalopa

295 was later diagnosed with diabetes insipidus, spastic quadriplegia, developmental delay, agenesis of t

296 ual disability, seizures, optic atrophy, and spastic quadriplegia.

297 nce); Ludvig and Sara Elsass Foundation, The Spastics Society and Vanforefonden (Denmark); Cooperativ

298 ticity, cognitive impairment, nystagmus, and spastic urinary bladder of varying severity.

299 distal esophageal spastic contractions) is a spastic variant with less favorable outcomes (66%) after

300 l disorders characterized by lower extremity spastic weakness.

301 l disorders characterized by lower extremity spastic weakness.